There is considerable evidence suggesting that the protein concentration of the plasma perfusing peritubular capillaries in the kidney is a major determinant of the sodium reabsorptive rate in the adjacent proximal tubules. It has been suggested that the oncotic effects of protein as well as hydrostatic pressure gradients alter the rate of emptying of the lateral intercellular spaces and this, by an unknown mechanism, alters net lumen-to-blood sodium transport. This hypothesis suggests that the rate of emptying of the lateral intercellular spaces is a major regulating determinant of isotonic transport. This would gain credence if other isotonically-transporting epithelia (in addition to the renal proximal tubule) showed these regulatory characteristics. The gall bladder mucosa transports sodium isotonically and would be an excellent model for these proposed studies. The effects of alterations of plasma oncotic pressure and hydrostatic pressure on the rate of sodium reabsorption of this organ would be evaluated. Since this tissue continues to transport salt and water in vitro, the role of oncotic and hydrostatic pressure gradients could be assessed separately. Furthermore, studies of the mechanisms by which these factors exert their effects would be simplified. Elucidation of the mechanism of control of solute reabsorption in this tissue may improve our understanding of the kidney and ultimately of abnormal renal sodium retention in conditions such as congestive heart failure.